Neurological picture. Horner's syndrome and ipsilateral tongue paresis due to carotid artery dissection.
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ABSTRACT:
SUBMITTER: Tijssen C
PROVIDER: S-EPMC2077779 | biostudies-literature | 2007 Apr
REPOSITORIES: biostudies-literature
Publications
Neurological picture. Horner's syndrome and ipsilateral tongue paresis due to carotid artery dissection.
Tijssen Cees C van Rooij Willem Jan WJ
Journal of neurology, neurosurgery, and psychiatry 20070401 4
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Project description:BackgroundCarotid artery dissection due to extension of aortic dissection (CAEAD) is a severe complication of acute aortic dissection. The risk of ischemic stroke is increased. Early sonographic detection and repeat evaluation are necessary to guide clinical management.Case presentationA 58-year-old male patient presents with sudden, tearing retrosternal pain. Point-of-care carotid ultrasound is used to establish the diagnosis of CAEAD. We describe a number of sonographic features and compare ultrasound to other imaging modalities.ConclusionsBedside carotid ultrasound enables rapid, sensitive and safe hemodynamic assessment, especially in critically ill patients.
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Project description:PurposeWe aimed to evaluate the long-term outcome of carotid endarterectomy (CEA) and carotid artery stenting (CAS) in patients who underwent both procedures on different sides.MethodsIn this single-center retrospective study (2001-2019), 117 patients (men, N = 78; median age at CEA, 64.4 [interquartile range {IQR}, 57.8-72.2] years; median age at CAS, 68.8 [IQR, 61.0-76.0] years) with ≥50% internal carotid artery stenosis who had CEA on one side and CAS on the other side were included. The risk of restenosis was estimated by treatment adjusted for patient and lesion characteristics.ResultsNeurological symptoms were significantly more common (41.9% vs 16.2%, P<0.001) and patients had a significantly shorter mean duration of smoking (30.2 [standard deviation {SD}, 22.2] years vs 31.8 [SD, 23.4] years, P<0.001), hypertension (10.1 [SD, 9.8] years vs 13.4 [SD, 9.1] years, P<0.001), hyperlipidemia (3.6 [SD, 6.6] years vs 5.0 [SD, 7.3] years, P = 0.001), and diabetes mellitus (3.9 [SD, 6.9] years vs 5.7 [SD, 8.9] years, P<0.001) before CEA compared to those before CAS. While the prevalence of heavily calcified stenoses on the operated side (25.6% vs 6.8%, P<0.001), the incidence of predominantly echogenic/echogenic plaques (53.0% vs 70.1%, P = 0.011) and suprabulbar lesions (1.7% vs 22.2%, P<0.001) on the stented side was significantly higher. Restenosis rates were 10.4% at 1 year, 22.3% at 5 years, and 33.7% at the end of the follow-up (at 11 years) for CEA, while these were 11.4%, 14.7%, and 17.2%, respectively, for CAS. Cox regression analysis revealed a significantly higher risk of restenosis (hazard ratio [HR], 1.80; 95% confidence interval [CI], 1.05-3.10; P = 0.030) for CEA compared to that for CAS. After adjusting for relevant confounding factors (smoking, hypertension, diabetes mellitus, calcification severity, plaque echogenicity, and lesion location), the estimate effect size materially did not change, although it did not remain statistically significant (HR, 1.85; 95% CI, 0.95-3.60; P = 0.070).ConclusionIntra-patient comparison of CEA and CAS in terms of restenosis tilts the balance toward CAS.
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Project description:Total arch replacement and stent trunk were performed for two patients. One of these underwent a total bilateral carotid artery replacement in anatomical position while the other underwent partial carotid artery dissection. The first patient demonstrated no neurological complication after surgery and a postoperative computed tomography angiography (CTA) showed bilateral common carotid artery patency. However, the second patient had neurological dysfunction after surgery, while a postoperative CTA showed occlusion of the left common carotid artery. Anatomical replacement for a common carotid artery dissection with thrombus has the potential to significantly improve cerebral perfusion and reduce postoperative neurological complications.
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Project description:IntroductionInternal carotid artery dissection (ICAD) is a rare cause of acute ischemic stroke with large vessel occlusion (AIS-LVO). We aimed investigating the impact on outcome of internal carotid artery (ICA) patency after mechanical thrombectomy (MT) for AIS-LVO due to occlusive ICAD.Patients and methodsWe included consecutive patients with AIS-LVO due to occlusive ICAD treated with MT from January 2015 to December 2020 in three European stroke centers. We excluded patients with unsuccessful intracranial reperfusion after MT (modified Thrombolysis in Cerebral Infarction (mTICI) score < 2b). We compared 3-month favorable clinical outcome rate, defined as a modified Rankin scale (mRS) score ⩽2, according to ICA status (patency vs occlusion) at the end of MT and at 24-h follow-up imaging, using univariate and multivariable models.ResultsAmong 70 included patients, ICA was patent in 54/70 (77%) at the end of MT, and in 36/66 (54.5%) patients with 24-h follow-up imaging. Among patients with ICA patency at the end of MT, 32% presented ICA occlusion at 24-h control imaging. Favorable 3-month outcome occurred in 41/54 (76%) patients with ICA patency post-MT and in 9/16 (56%) patients with occluded ICA post-MT (p = 0.21). Rates of favorable outcome were significantly higher in patients with 24-h ICA patency compared to patients with 24-h ICA occlusion (32/36 [89%] vs 15/30 [50%]), with an adjusted odds ratio of 4.67 (95% CI: 1.26-17.25).Discussion and conclusionObtaining sustained (24-h) ICA patency after MT could be a therapeutic target for improving functional outcome in patients with AIS-LVO due to ICAD.
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Project description: Not available
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Project description:BackgroundAcute tandem cervical dissecting internal carotid artery (ICA) occlusion and intracranial embolic middle cerebral artery (MCA) occlusion can be devastating, and the optimal treatment strategy for this condition has not been established yet.Case descriptionA 45-year-old male presented with aphasia and right hemiparesis preceded by neck pain. Computed tomography showed a high-density signal along the left MCA, suggesting extensive emboli. Magnetic resonance angiography demonstrated tandem occlusion of the left cervical ICA and intracranial MCA with minimal diffusion-weighted imaging lesion. Emergent surgical embolectomy was performed, and long intracranial MCA emboli were retrieved with collateral cross-flow restoration. The cervical ICA was exposed, and dissection was confirmed. The cervical ICA was ligated, and superficial temporal artery (STA)-MCA anastomosis was added. Postoperatively, the patient demonstrated recovery from right hemiparesis and aphasia. At the 6(th) postoperative month, follow-up studies demonstrated a robustly patent STA-MCA bypass and no additional ischemic lesion on T2-weighted imaging.ConclusionsSurgical embolectomy in conjunction with ligation of the cervical ICA followed by STA-MCA bypass might be a safe alternative method to endovascular recanalization, when the cervical dissection is extensive and when huge secondary emboli are present along the MCA.
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Project description:BackgroundThe emergence of neurologic symptoms after carotid revascularization is not uncommon and typically caused by perioperative ischemic stroke or hyperperfusion. Postoperative vasculopathy, including reversible cerebral vasoconstriction syndrome (RCVS) is a rare complication of carotid intervention and may be an under-identified cause of neurologic deficit after revascularization. We report a case of reversible postoperative vasculopathy following carotid revascularization as well as its management.Case presentationA 74 year old right-handed woman presented to the emergency department with sudden onset left arm weakness and episodic shaking while hypotensive. Computed tomography angiography revealed total occlusion of her right internal carotid artery. Transcranial Doppler monitoring demonstrated active embolic events in her right middle cerebral artery raising concern for continued stump embolization. She underwent carotid revascularization with carotid endarterectomy, mechanical thrombectomy, and carotid angioplasty and initially did well postoperatively. On postoperative day 5, she developed a fixed right gaze and left hemiparesis. Computed tomography revealed new right frontal lobe and basal ganglia infarcts, and angiography showed new right internal carotid, middle cerebral, and anterior cerebral artery vasoconstriction consistent with postoperative vasculopathy. Despite treatment with pressure augmentation and vasodilator therapy, her symptoms persisted resulting in left hemiplegia at discharge.DiscussionThis case highlights postoperative vasculopathy (including RCVS) as a rare potential complication after carotid revascularization that should be considered in a patient with persistent acute neurologic symptoms. Information regarding incidence and predisposing risk factors is limited. Multiple diagnostic and therapeutic modalities may be necessary in the recognition and treatment of postoperative vasculopathy.
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